Hanesworth J M, Sardinia M F, Krebs L T, Hall K L, Harding J W
Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, College of Veterinary Medicine, Washington State University, Pullman.
J Pharmacol Exp Ther. 1993 Aug;266(2):1036-42.
Data are presented describing a new angiotensin binding site in rabbit and guinea pig heart, distinct from AT1 and AT2, that demonstrates high specificity and affinity for the hexapeptide fragment angiotensin II(3-8), which will be referred to here as angiotensin IV (AIV). Equilibrium binding in rabbit heart membranes was achieved in 2 hr at 37 degrees C and produced a calculated kinetic KD of .174 +/- .018 nM. Saturation equilibrium binding data for rabbit and guinea pig heart were best fit to a one-site model with Hill coefficients near unity. Guinea pig membranes exhibited a KD = 1.33 +/- .02 nM and a Bmax = 144 +/- 19 fmol/mg protein, and rabbit heart membranes had a KD = 1.70 +/- .50 nM and a Bmax = 731 +/- 163 fmol/mg protein. The binding site showed a high specificity for AIV, although it exhibited low affinity for angiotensin II, angiotensin III, Sar1,Ile8-angiotensin II, DuP 753, CGP42112A and PD123177. A large number of nonangiotensin-related peptides were unable to compete effectively for 125I-AIV binding. Deletions made from the C-terminal end of AIV caused a decrease in affinity: AIV > AII(3-7) >> AII(3-6) >> AII(3-5). Extension of the C-terminal end of AIV corresponding to the amino acids of human angiotensinogen caused little change in affinity. GTP gamma S had no effect on binding, suggesting non-G protein linkage. Binding was widely distributed throughout the heart; it was observed on cardiocytes and blood vessels as well as in the epicardium and the endocardium.
本文呈现的数据描述了兔和豚鼠心脏中一种新的血管紧张素结合位点,该位点不同于AT1和AT2,对六肽片段血管紧张素II(3 - 8)表现出高特异性和亲和力,在此将其称为血管紧张素IV(AIV)。兔心脏膜中的平衡结合在37℃下2小时内达到,计算得出的动力学KD为0.174±0.018 nM。兔和豚鼠心脏的饱和平衡结合数据最适合单一位点模型,希尔系数接近1。豚鼠膜的KD = 1.33±0.02 nM,Bmax = 144±19 fmol/mg蛋白质,兔心脏膜的KD = 1.70±0.50 nM,Bmax = 731±163 fmol/mg蛋白质。该结合位点对AIV具有高特异性,尽管它对血管紧张素II、血管紧张素III、Sar1,Ile8 - 血管紧张素II、DuP 753、CGP42112A和PD123177的亲和力较低。大量非血管紧张素相关肽不能有效竞争125I - AIV的结合。从AIV的C末端进行缺失会导致亲和力下降:AIV > AII(3 - 7) >> AII(3 - 6) >> AII(3 - 5)。将AIV的C末端延伸至与人血管紧张素原氨基酸对应的部分,亲和力变化不大。GTPγS对结合无影响,表明不存在G蛋白连接。结合广泛分布于整个心脏;在心肌细胞、血管以及心外膜和心内膜中均有观察到。